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and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T91","span":{"begin":101,"end":121},"obj":"Protein"},{"id":"T92","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T93","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T94","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T95","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T96","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T97","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T98","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T99","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T100","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T101","span":{"begin":1160,"end":1164},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T625","span":{"begin":124,"end":128},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T626","span":{"begin":306,"end":310},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T627","span":{"begin":455,"end":459},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T628","span":{"begin":482,"end":486},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T629","span":{"begin":554,"end":558},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T630","span":{"begin":803,"end":807},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T631","span":{"begin":1160,"end":1164},"obj":"http://www.uniprot.org/uniprot/O00206"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"UBERON-AE","denotations":[{"id":"T62","span":{"begin":695,"end":701},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T61","span":{"begin":520,"end":527},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T60","span":{"begin":1284,"end":1289},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T59","span":{"begin":1074,"end":1079},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T58","span":{"begin":514,"end":519},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T57","span":{"begin":271,"end":276},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"GO-BP","denotations":[{"id":"T102","span":{"begin":0,"end":12},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T103","span":{"begin":237,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T104","span":{"begin":53,"end":65},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T105","span":{"begin":342,"end":354},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T106","span":{"begin":1209,"end":1221},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T107","span":{"begin":170,"end":179},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T108","span":{"begin":325,"end":334},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T109","span":{"begin":501,"end":510},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T110","span":{"begin":1179,"end":1188},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T111","span":{"begin":223,"end":233},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T112","span":{"begin":223,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0002676"},{"id":"T113","span":{"begin":223,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0050729"},{"id":"T114","span":{"begin":223,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0050727"},{"id":"T115","span":{"begin":223,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0050728"},{"id":"T116","span":{"begin":223,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0002673"},{"id":"T117","span":{"begin":568,"end":596},"obj":"http://purl.obolibrary.org/obo/GO_0006468"},{"id":"T118","span":{"begin":581,"end":596},"obj":"http://purl.obolibrary.org/obo/GO_0016310"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"sentences","denotations":[{"id":"T71","span":{"begin":1120,"end":1297},"obj":"Sentence"},{"id":"T70","span":{"begin":1007,"end":1119},"obj":"Sentence"},{"id":"T69","span":{"begin":769,"end":1006},"obj":"Sentence"},{"id":"T64","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T65","span":{"begin":101,"end":277},"obj":"Sentence"},{"id":"T66","span":{"begin":278,"end":378},"obj":"Sentence"},{"id":"T67","span":{"begin":379,"end":553},"obj":"Sentence"},{"id":"T68","span":{"begin":554,"end":768},"obj":"Sentence"},{"id":"T3","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T4","span":{"begin":101,"end":277},"obj":"Sentence"},{"id":"T5","span":{"begin":278,"end":378},"obj":"Sentence"},{"id":"T6","span":{"begin":379,"end":553},"obj":"Sentence"},{"id":"T7","span":{"begin":554,"end":768},"obj":"Sentence"},{"id":"T8","span":{"begin":769,"end":1006},"obj":"Sentence"},{"id":"T9","span":{"begin":1007,"end":1119},"obj":"Sentence"},{"id":"T10","span":{"begin":1120,"end":1297},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"simple1","denotations":[{"id":"T154","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T153","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T152","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T151","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T150","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T149","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T148","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T147","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T146","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T145","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T144","span":{"begin":101,"end":121},"obj":"Protein"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T738","span":{"begin":1057,"end":1066},"obj":"Positive_regulation"},{"id":"T737","span":{"begin":839,"end":848},"obj":"Positive_regulation"},{"id":"T736","span":{"begin":922,"end":931},"obj":"Negative_regulation"},{"id":"T735","span":{"begin":942,"end":952},"obj":"Positive_regulation"},{"id":"T734","span":{"begin":581,"end":596},"obj":"Phosphorylation"},{"id":"T733","span":{"begin":441,"end":451},"obj":"Gene_expression"},{"id":"T732","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T731","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T730","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T729","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T728","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T727","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T726","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T725","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T724","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T723","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T722","span":{"begin":101,"end":121},"obj":"Protein"}],"relations":[{"id":"R509","pred":"themeOf","subj":"T725","obj":"T733"},{"id":"R510","pred":"themeOf","subj":"T727","obj":"T734"},{"id":"R511","pred":"themeOf","subj":"T728","obj":"T734"},{"id":"R512","pred":"themeOf","subj":"T730","obj":"T737"},{"id":"R513","pred":"themeOf","subj":"T730","obj":"T736"},{"id":"R514","pred":"themeOf","subj":"T730","obj":"T735"},{"id":"R515","pred":"themeOf","subj":"T731","obj":"T738"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"BioNLP16_Messiy","denotations":[{"id":"T633","span":{"begin":101,"end":121},"obj":"Protein"},{"id":"T634","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T635","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T636","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T637","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T638","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T639","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T640","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T641","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T642","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T643","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T645","span":{"begin":441,"end":451},"obj":"Gene_expression"},{"id":"T646","span":{"begin":581,"end":596},"obj":"Phosphorylation"},{"id":"T647","span":{"begin":922,"end":931},"obj":"Negative_regulation"},{"id":"T648","span":{"begin":942,"end":952},"obj":"Positive_regulation"},{"id":"T649","span":{"begin":839,"end":848},"obj":"Positive_regulation"}],"relations":[{"id":"R529","pred":"themeOf","subj":"T636","obj":"T645"},{"id":"R530","pred":"themeOf","subj":"T638","obj":"T646"},{"id":"R531","pred":"themeOf","subj":"T639","obj":"T646"},{"id":"R532","pred":"themeOf","subj":"T641","obj":"T647"},{"id":"R533","pred":"themeOf","subj":"T641","obj":"T648"},{"id":"R534","pred":"themeOf","subj":"T641","obj":"T649"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

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Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T142","span":{"begin":1174,"end":1178},"obj":"Protein"},{"id":"T141","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T140","span":{"begin":1057,"end":1066},"obj":"Positive_regulation"},{"id":"T139","span":{"begin":1047,"end":1051},"obj":"Protein"},{"id":"T138","span":{"begin":1020,"end":1026},"obj":"Protein"},{"id":"T137","span":{"begin":922,"end":931},"obj":"Negative_regulation"},{"id":"T136","span":{"begin":839,"end":848},"obj":"Positive_regulation"},{"id":"T135","span":{"begin":803,"end":812},"obj":"Protein"},{"id":"T134","span":{"begin":662,"end":670},"obj":"Positive_regulation"},{"id":"T133","span":{"begin":662,"end":670},"obj":"Positive_regulation"},{"id":"T132","span":{"begin":581,"end":596},"obj":"Phosphorylation"},{"id":"T131","span":{"begin":652,"end":656},"obj":"Protein"},{"id":"T130","span":{"begin":554,"end":563},"obj":"Protein"},{"id":"T129","span":{"begin":441,"end":451},"obj":"Gene_expression"},{"id":"T128","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T127","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T126","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T125","span":{"begin":320,"end":324},"obj":"Protein"},{"id":"T124","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T123","span":{"begin":164,"end":168},"obj":"Protein"},{"id":"T122","span":{"begin":140,"end":162},"obj":"Protein"}],"relations":[{"id":"R21","pred":"themeOf","subj":"T132","obj":"T134"},{"id":"R18","pred":"themeOf","subj":"T126","obj":"T129"},{"id":"R19","pred":"themeOf","subj":"T130","obj":"T132"},{"id":"R20","pred":"themeOf","subj":"T130","obj":"T133"},{"id":"R22","pred":"themeOf","subj":"T135","obj":"T136"},{"id":"R23","pred":"themeOf","subj":"T135","obj":"T137"},{"id":"R24","pred":"themeOf","subj":"T138","obj":"T140"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"testone","denotations":[{"id":"T28","span":{"begin":1057,"end":1066},"obj":"Positive_regulation"},{"id":"T27","span":{"begin":922,"end":931},"obj":"Negative_regulation"},{"id":"T26","span":{"begin":839,"end":848},"obj":"Positive_regulation"},{"id":"T25","span":{"begin":441,"end":451},"obj":"Gene_expression"},{"id":"T24","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T23","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T22","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T21","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T20","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T19","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T18","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T17","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T16","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T15","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T14","span":{"begin":101,"end":121},"obj":"Protein"}],"relations":[{"id":"R1","pred":"equivalentTo","subj":"T15","obj":"T14"},{"id":"R2","pred":"themeOf","subj":"T17","obj":"T25"},{"id":"R3","pred":"equivalentTo","subj":"T21","obj":"T20"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}

{"project":"test3","denotations":[{"id":"T40","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T39","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T38","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T37","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T36","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T35","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T34","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T33","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T32","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T31","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T30","span":{"begin":101,"end":121},"obj":"Protein"},{"id":"T55","span":{"begin":1160,"end":1164},"obj":"Protein"},{"id":"T54","span":{"begin":1022,"end":1026},"obj":"Protein"},{"id":"T53","span":{"begin":922,"end":931},"obj":"Negative_regulation"},{"id":"T52","span":{"begin":839,"end":848},"obj":"Positive_regulation"},{"id":"T51","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T50","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T49","span":{"begin":600,"end":621},"obj":"Protein"},{"id":"T48","span":{"begin":554,"end":558},"obj":"Protein"},{"id":"T47","span":{"begin":482,"end":486},"obj":"Protein"},{"id":"T46","span":{"begin":455,"end":459},"obj":"Protein"},{"id":"T45","span":{"begin":441,"end":451},"obj":"Gene_expression"},{"id":"T44","span":{"begin":306,"end":310},"obj":"Protein"},{"id":"T43","span":{"begin":124,"end":128},"obj":"Protein"},{"id":"T42","span":{"begin":101,"end":121},"obj":"Protein"}],"relations":[{"id":"R4","pred":"equivalentTo","subj":"T43","obj":"T42"},{"id":"R5","pred":"themeOf","subj":"T46","obj":"T45"},{"id":"R6","pred":"equivalentTo","subj":"T50","obj":"T49"},{"id":"R7","pred":"themeOf","subj":"T51","obj":"T52"},{"id":"R8","pred":"themeOf","subj":"T51","obj":"T53"}],"text":"Inflammation and immunity play a crucial role in the pathogenesis of Intracerebral hemorrhage (ICH). Toll-like receptor 4- (TLR4-) mediated nuclear factor kappa-B (NFκB) signaling plays critical roles in the activation and regulation of inflammatory responses in injured brain. However, the involvement of TLR4-mediated NFκB signaling in the pathogenesis of ICH remains unknown. The present study was to evaluate the temporal profile of the expression of TLR4 and the activation of TLR4-mediated NFκB signaling in brain tissues of Wistar rats after ICH. TLR4 mRNA and protein, the phosphorylation of inhibitors of kappa B (p-IκBα), and the activity of NFκB were examined in hemorrhagic cerebral tissue by Rt-PCR, Western blots, immunohistochemistry staining, and EMSA. Compared with saline control, the TLR4 mRNA and protein significantly increased starting at 6 hours after ICH, peaked on the 3rd day after ICH, and then decreased but still maintained at a higher level on the 7th day after ICH (P \u003c .05). The level of p-IκBα and the activity of NFκB also increased in the brain after ICH compared with saline control. The present study firstly suggests that TLR4-mediated NFκB signaling participates in the pathogenesis of ICH, which may become a therapeutic target for ICH-induced brain damage."}